Development of transneuronal, secondary, injuries developing in distant but anatomically connected regions following primary, direct injury to the cerebral cortex was shown to be associated with an abnormal uptake of calcium, and blood-brain barrier (BSSB) permeability changes in those areas. The delayed onset of these changes, pattern of calcium uptake into dendritic structures, and intracytoplasmic uptake of extravasated albumin suggest a neuroexcitatory nature of mechanisms involved. If correct, studies will be developed to ascertain whether suppression or reduction of neuroexcitation by some agents could substantially ameliorate or prevent development of secondary transneuronal injuries. This could be of relevance to the treatment of brain trauma patients.